Isomer-sourced structure iteration methods for in silico development of inhibitors: Inducing GTP-bound NRAS-Q61 oncogenic mutations to an “off-like” state

The NRAS-mutant subset of melanoma represent some of the most aggressive and deadliest types associated with poor overall survival. Unfortunately, for more than 40 years, no therapeutic agent directly targeting NRAS mutations has been clinically approved. In this work, based on microsecond scale mol...

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Detalles Bibliográficos
Autores: Hu, Zheyao, Martí Rabassa, Jordi|||0000-0002-3721-9634
Tipo de recurso: artículo
Fecha de publicación:2024
País:España
Institución:Universitat Politècnica de Catalunya (UPC)
Repositorio:UPCommons. Portal del coneixement obert de la UPC
Idioma:inglés
OAI Identifier:oai:upcommons.upc.edu:2117/408734
Acceso en línea:https://hdl.handle.net/2117/408734
https://dx.doi.org/10.1016/j.csbj.2024.05.038
Access Level:acceso abierto
Palabra clave:Drugs--Design
Oncogenes
Molecular mechanisms
Drug design
NRAS oncogenes
ISSI method
HM-387 compound
Medicaments--Disseny
Oncogens
Àrees temàtiques de la UPC::Física
Descripción
Sumario:The NRAS-mutant subset of melanoma represent some of the most aggressive and deadliest types associated with poor overall survival. Unfortunately, for more than 40 years, no therapeutic agent directly targeting NRAS mutations has been clinically approved. In this work, based on microsecond scale molecular dynamics simulations, the effect of Q61 mutations on NRAS conformational characteristics is revealed at the atomic level. The GTP-bound NRAS-Q61R and Q61K mutations show a specific targetable pocket between Switch-II and a-helix 3 whereas the NRAS-Q61L non-polar mutation category shows a different targetable pocket. Moreover, a new isomer-sourced structure iteration method has been developed for the in silico design of a potential inhibitor prototype (HM-387) capable of targeting NRAS-Q61R proteins. We also show the possibility of HM-387 targeting activated NRAS-Q61R and that it can gradually induce the transition of an activated NRAS-Q61R to an “off-like” state.